Q-omics provides the consensus-scored SENP8 profile across patient tissues and cancer cell-line models. SENP8 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SENP8 is differentially expressed in 10, with the highest sampling consensus in THCA. Additionally, SENP8 protein abundance shows 21,946 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, THCA, and LUAD as cancer lineages where SENP8 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for SENP8 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SENP8 survival associations across molecular data types. SENP8 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SENP8 RNA expression–survival associations across cancer types. High SENP8 expression shows unfavorable associations in UVM and SCLC, but favorable associations in KIRC, COAD, KIRP and READ. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for SENP8 RNA expression.
This table summarizes SENP8 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for SENP8. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SENP8 shows lower tumor expression in THCA, COAD, KICH, KIRP, KIRC and LUSC. The THCA box plot shows higher SENP8 RNA expression in normal versus tumor tissue (log2 FC = −1.340, t-test p < 0.001).
This table shows molecular features associated with SENP8 in patient tissues and cancer cell lines. In patient samples, SENP8 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SENP8 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
